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Despite the abundance of research on the determinants of eco-innovation, there are few studies dealing with the case of developing countries. This paper contributes to the empirical literature on the determinants of eco-innovation through a survey of 159 Tunisian industrial firms, 61 of which identify themselves as eco-innovators. The objective is to test the influence of the determinants of eco-innovation: regulatory instruments, market instruments, technology, expected benefits, and consumer demand on eco-innovation behaviour. The data were processed using principal component analysis and discriminant analysis. The results show that technology, competitive pressure, expected benefits, and market instruments stimulate eco-innovation in the Tunisian context. However, regulatory instruments and ecological consumer demand do not contribute significantly. These results have important implications for both policymakers and business managers.

New multiple sclerosis (MS) disease-modifying therapies (DMTs), which exert beneficial effects through prevention of relapse, limitation of disability progression, and improvement of patients’ quality of life, have recently emerged. Nonetheless, these DMTs are not without associated complications (severe adverse events like. progressive multifocal leukoencephalopathy). Patient follow-up requires regular clinical evaluations and close monitoring with magnetic resonance imaging (MRI). Detection of new T2 lesions and potential brain atrophy measurements contribute to the evaluation of treatment effectiveness. Current MRI protocols for MS recommend the acquisition of an annual gadolinium (Gd) enhanced MRI, resulting in administration of high volume of contrast agents over time and Gd accumulation in the brain.

Outre son rôle dans l’érythropoïèse, l’érythropoïétine (Epo) joue un rôle dans la protection tissulaire, notamment par des effets cardioprotecteurs, néphroprotecteurs et neuroprotecteurs. La présence de l’Epo et de son récepteur (Epo-R) dans le tissu pulmonaire suggère également un effet cytoprotecteur dans le poumon. Notre projet vise à documenter ce rôle en utilisant un modèle murin sous-exprimant l’Epo. Les résultats obtenus permettront de mieux comprendre les effets cytoprotecteurs de l’Epo mais également d’apprécier ses effets bénéfiques dans le cas d’atteintes du poumon distal.

Fall of the elderly person is a public health problem. The objectives of our study were to evaluate the relevance of systematically performing in emergency a computed tomography (CT) scan for fall in the elderly person, to identify specific criteria predicting the appearance of lesions.

Obstructive Sleep Apnea syndrome (OSA) is frequently associated with idiopathic pulmonary fibrosis (IPF). Nocturnal Intermittent hypoxia (IH), the main pathogenic trait of OSA, has been shown to be a pejorative prognostic factor in IPF. Previous studies from our lab demonstrated that the severity of mouse pulmonary fibrosis induced by bleomycin (BLM) was more pronounced when mice were also exposed to IH, and that this effect was exacerbated when IH exposure preceded the onset of fibrosis. In the latter study, we have also shown that this effect was associated with an increase in ER stress markers ATF6 and XBP-1 1. Interestingly, the use of tauroursodeoxycholic acid (TUDCA), a chemical chaperone that reduces ER stress by facilitating proper protein folding and trafficking, suppresses IH-induced apoptosis and fibrosis in mouse pulmonary tissues 2. The aim of our study was to investigate the implication of IH-induced ER stress in the pro-fibrotic and overall worsening effect of HI on BLM-induced lung fibrosis and to decipher the specific targeted pathways involved in this effect.

La commande centrale respiratoire est élaborée par un réseau de neurones localisé au niveau du pont et du bulbe rachidien. L’activité de ce réseau est modulée en permanence par des afférences centrale et périphérique provenant d’éléments de régulations tels que les chémorécepteurs. La chémoréception respiratoire centrale et périphérique est cruciale pour maintenir l’homéostasie en oxygène (O2) et en dioxyde de carbone (CO2). En régulant le potentiel de repos membranaire au niveau des structures centrales et périphériques, le canal potassique KCNK3/TASK-1 semble jouer un rôle important dans cette chémoréception, cependant, des Résultats controversés existent dans la littérature.

La fibrose pulmonaire idiopathique (FPI) est une pneumopathie interstitielle de cause inconnue. Certains patients présentent une atteinte ventilatoire caractérisée par une faible valeur de capacité vitale forcée associée à une augmentation de la fréquence respiratoire (fR) et une diminution du volume courant (VT), ainsi qu’une dyspnée. Une étude menée au laboratoire sur un modèle murin de fibrose pulmonaire induite par instillations intra-trachéale répétées de Bléomycine (BLM) a montré qu’une fibrose pulmonaire sévère induit une neuroplasticité au niveau du réseau neuronal respiratoire à l’origine de la commande centrale respiratoire. Par ailleurs, 62 % des patients FPI présentent un syndrome d’apnée obstructif du sommeil (SAOS) modéré à sévère et nous avons démontré expérimentalement qu’une pré-exposition à l’hypoxie intermittente chronique (HIC), élément délétère du SAOS, aggravait la fibrose pulmonaire. Ainsi, nous suggérons que les atteintes pulmonaires liées à la fibrose d’une part et l’exposition à l’HIC d’autre part puisse avoir des effets additionnels sur le fonctionnement du réseau neuronal respiratoire.

Il termine idrocefalo indica una situazione di eccesso di liquido cerebrospinale (LCS) nei ventricoli cerebrali, diversa rispetto alla dilatazione passiva dei ventricoli. Dietro alla sua apparente semplicità, questo termine racchiude delle entità molto eterogenee. Idrocefali molto diversi possono, così, essere distinti in base all’età dei pazienti (idrocefalo del bambino/idrocefalo dell’adulto), al loro meccanismo (difetto di assorbimento, disturbi della circolazione del LCS o, più raramente, produzione in eccesso), all’esistenza o meno di un ostacolo al flusso del LCS (idrocefalo comunicante o non comunicante) e, infine, in base alle loro modalità di installazione (idrocefalo acuto/idrocefalo cronico). Il nostro obiettivo, qui, è di descrivere le diverse forme cliniche di idrocefalo nei bambini e negli adulti e la loro fisiopatologia. Definiremo, poi, gli esami complementari a nostra disposizione: imaging, biomarcatori, ma anche puntura lombare ed esplorazione idrodinamica del LCS. Vedremo che l’idrocefalo a pressione normale, o idrocefalo cronico degli adulti, è un’entità molto particolare, che solleva problemi specifici di diagnosi e di decisione terapeutica. Infine, descriveremo i trattamenti, soprattutto chirurgici, a nostra disposizione, le loro indicazioni e i loro risultati, sottolineando la necessità di mantenere a lungo termine il follow-up clinico dei pazienti operati.

Most fisheries worldwide remunerate their crew with a share system, where crew receive a part of the revenues or a part of the revenues less costs, rather than a fixed wage. Although labor is one of the main costs in fisheries and the share remuneration system has a strong influence on firm behavior and its economic performance, little attention has been paid it. In a share remuneration system, crew salaries can significantly increase when the economic performance of a vessel improves. This allows the crew to capture part of the fisheries rent. Bioeconomic analyses are performed for the Bay of Biscay nephropsfishery on main management targets. Results confirm the importance of considering a share system compared to a fixed remuneration system in vessel owner (capital) and crew (labor) rent distribution and fishing decisions.

Abstract This article investigates the relationship between optimal gear selectivity and effort cost in the fishing industry. We first show that optimal selectivity depends negatively on the level of effort cost, but that this relationship is not continuous. Optimal selectivity switches when real effort cost goes beyond a certain level, and this switch induces a non-marginal reduction in the level of fishing effort. In the second part of this article, we show that the current level of real effort cost in the Nephrops fishery of the Bay of Biscay is far below the switch point, which makes high selectivity optimal. The discrepancy between optimal and current selectivity may be explained by the state of the fishery management and also by the fact that selectivity is hardly observable with the type of gear presently used.

Le transport ionique de sodium (Na+) par les cellules épithéliales des poumons permet de réguler la quantité de liquide des voies aériennes et permet la résorption du liquide du poumon à la naissance, ainsi que de l’oedème pulmonaire chez l’adulte. Ce transport est modulé en grande partie par le canal ionique ENaC (epithelial Na channel). Si l’augmentation de l’activité de ENaC dans les voies aériennes se traduit par une accumulation de mucus et une inflammation comme dans la fibrose kystique, l’inhibition de ENaC dans les alvéoles lors d’une infection pulmonaire pourrait contribuer à aggraver la sévérité d’un syndrome de détresse respiratoire. Les stratégies pharmacologiques qui modulent l’activité ou l’expression du canal ENaC pourraient donc être bénéfiques dans différentes pathologies pulmonaires.

Sodium 4-phenylbutyrate (4-PBA) has attracted a great deal of attention in cystic fibrosis (CF) pathology due to its capacity to traffic ΔF508-cystic fibrosis transmembrane conductance regulator (CFTR) to the cell membrane and restore CFTR chloride function at the plasma membrane of CF lung cells in vitro and in vivo. Using two different ΔF508-CFTR lung epithelial cell lines (CFBE41o- and IB3-1 cells, characterized with ΔF508-homozygous and heterozygous genotype, respectively) in vitro, 4-PBA induced an increase of proinflammatory cytokine interleukin (IL)-8 production in a concentration-dependent manner. This 4-PBA-induced IL-8 production was associated with a strong reduction of proteasome and nuclear factor-κB transcriptional activities in the two ΔF508-CFTR lung cells either in a resting state or after tumor necrosis factor-α stimulation. In contrast, a strong increase of activator protein-1 transcriptional activity was observed. The inhibition of extracellular signal-regulated protein kinase 1/2 (ERK1/2) by 1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio] butadiene (U0126) and 2-(2-amino-3-methoxyphenyl)-4 H-1-benzopyran-4-one (PD98059) and c-Jun-NH2-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) by anthra[1,9-cd] pyrazol-6 (2 H)-one (SP600125), respectively, was associated with a reduction (2–3.5-fold) of IL-8 production in both ΔF508-CFTR lung cell lines treated with 4-PBA. No significant change of IL-8 production was observed after an inhibition of p38 MAPK with 4-[4-(4-fluorophenyl)-5-(4-pyridinyl)-1 H-imidazol-2-yl] phenol (SB202190). Therefore, we suggest that inhibition of both ERK1/2 and JNK signaling may be a means to strongly reduce 4-PBA-induced IL-8 production in combination with 4-PBA treatment to restore CFTR Cl-channel function in lung epithelial cells of patients with CF.

Sodium 4-phenylbutyrate (4-PBA) has attracted a great deal of attention in cystic fibrosis (CF) pathology due to its capacity to traffic DeltaF508-cystic fibrosis transmembrane conductance regulator (CFTR) to the cell membrane and restore CFTR chloride function at the plasma membrane of CF lung cells in vitro and in vivo. Using two different DeltaF508-CFTR lung epithelial cell lines (CFBE41o- and IB3-1 cells, characterized with DeltaF508-homozygous and heterozygous genotype, respectively) in vitro, 4-PBA induced an increase of proinflammatory cytokine interleukin (IL)-8 production in a concentration-dependent manner. This 4-PBA-induced IL-8 production was associated with a strong reduction of proteasome and nuclear factor-kappaB transcriptional activities in the two DeltaF508-CFTR lung cells either in a resting state or after tumor necrosis factor-alpha stimulation. In contrast, a strong increase of activator protein-1 transcriptional activity was observed. The inhibition of extracellular signal-regulated protein kinase 1/2 (ERK1/2) by 1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio] butadiene (U0126) and 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) and c-Jun-NH(2)-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) by anthra[1,9-cd] pyrazol-6 (2H)-one (SP600125), respectively, was associated with a reduction (2-3.5-fold) of IL-8 production in both DeltaF508-CFTR lung cell lines treated with 4-PBA. No significant change of IL-8 production was observed after an inhibition of p38 MAPK with 4-[4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazol-2-yl] phenol (SB202190). Therefore, we suggest that inhibition of both ERK1/2 and JNK signaling may be a means to strongly reduce 4-PBA-induced IL-8 production in combination with 4-PBA treatment to restore CFTR Cl(-) channel function in lung epithelial cells of patients with CF.

Cystic fibrosis is a lethal inherited disorder caused by mutations in a single gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) protein, resulting in progressive oxidative lung damage. In this study, we evaluated the role of CFTR in the control of ubiquitin-proteasome activity and nuclear factor (NF)-κB/IκB-α signaling after lung oxidative stress. After a 64-hour exposure to hyperoxia-mediated oxidative stress, CFTR-deficient (cftr−/−) mice exhibited significantly elevated lung proteasomal activity compared with wild-type (cftr+/+) animals. This was accompanied by reduced lung caspase-3 activity and defective degradation of NF-κB inhibitor IκB-α. In vitro, human CFTR-deficient lung cells exposed to oxidative stress exhibited increased proteasomal activity and decreased NF-κB-dependent transcriptional activity compared with CFTR-sufficient lung cells. Inhibition of the CFTR Cl−channel by CFTRinh-172in the normal bronchial immortalized cell line 16HBE14o− increased proteasomal degradation after exposure to oxidative stress. Caspase-3 inhibition by Z-DQMD in CFTR-sufficient lung cells mimicked the response profile of increased proteasomal degradation and reduced NF-κB activity observed in CFTR-deficient lung cells exposed to oxidative stress. Taken together, these results suggest that functional CFTR Cl−channel activity is crucial for regulation of lung proteasomal degradation and NF-κB activity in conditions of oxidative stress.

This paper deals with the economic impact of the invasion of a scallop fishery by an exotic shellfish that was accidentally imported some decades ago. The invasive alien species, a slipper-limpet, Crepidula fornicata,is a space competitor for local scallops, and its spread threatens the sustainability of the ongoing scallop restocking program. Facing this invasion, the local fisheries committee has initiated a containment project intending to make the restocking program consistent with the exotic species presence in the fishery. The issue is complicated by the occurrence of occasional toxic micro-algae blooms affecting the scallop fishery. The paper presents a model dealing with the economic impact of the invasive process, and a methodology for cost-benefit analysis of invasion management. According to numerical simulation, the invasion is a serious threat to the economic viability of the restocking program, and invasion management would help maintaining the long term sustainability of the fishery. Sensitivity tests highlight the importance of long term equilibrium scallop catches on the program result, depending on scallop farming technical performance and ecosystem disturbance.